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Hypertension-induced remodelling: on the interactions of cardiac risk factors
1Department of Physiology Anatomy and Genetics, University of Oxford, Oxford, UK.
Insights
Hypertension causes cardiac remodelling and sympathetic nervous system changes, increasing heart disease risk. This review explores their complex interactions, revealing potential compensatory roles and relevance beyond hypertension.
Area of Science:
- Cardiovascular Science
- Pathophysiology
- Medical Research
Background:
- Hypertension triggers cardiac remodelling, including hypertrophy and fibrosis, and alters sympathetic nervous system activity.
- These changes are known risk factors for severe heart diseases like congestive heart failure and ventricular fibrillation.
- Existing research often studies these factors in isolation, neglecting their intricate interactions.
Purpose of the Study:
- To conduct a comprehensive review of the interactions between hypertension-induced cardiac remodelling, sympathetic nervous system activity, and heart diseases.
- To introduce a framework for understanding these complex relationships and their clinical implications.
- To explore the potential compensatory roles of certain mechanisms and their relevance in other cardiac conditions.
Main Methods:
- Multiscale literature review focusing on the interplay between cardiac remodelling, sympathetic nervous system activity, and heart diseases.
- Development of a conceptual framework to analyze and visualize these interactions.
- Analysis of existing evidence to re-evaluate the pathological versus compensatory nature of specific mechanisms.
Main Results:
- Identified numerous, often overlooked, interactions between hypertension-induced cardiac changes and heart disease progression.
- Demonstrated that cardiac fibrosis and elevated sympathetic nervous system activity may serve compensatory functions in certain contexts.
- Highlighted the clinical relevance of these interactions for therapeutic outcomes and mortality in hypertensive patients.
Conclusions:
- Understanding the complex interactions between cardiac remodelling, fibrosis, and sympathetic activity is crucial for effective hypertension management.
- These mechanisms are not solely pathological and can play compensatory roles, influencing therapeutic strategies.
- The identified interactions are also relevant to conditions beyond hypertension, such as healed myocardial infarction.
Abstract:
Hypertension induces considerable cardiac remodelling, such as hypertrophy, interstitial fibrosis, and abnormal activity of the cardiac sympathetic nervous system, which are established risk factors in several highly dangerous heart diseases, such as ventricular fibrillation and congestive heart failure. All these risk factors and heart diseases are studied extensively in isolation, but to our knowledge, there is no comprehensive review of their interactions. At the same time, there is growing evidence suggesting that such interactions are numerous and that a successful therapy against a particular condition may have unexpectedly weak effects on mortality, as treated patients may die of a different cause exacerbated by the therapy. In this article, we present a multiscale review of the literature focusing on the relationships between the above-mentioned risk factors and heart diseases, and introduce a framework that gives insight into their possible interactions. We use this framework to demonstrate that conditions such as fibrosis and elevated activity of the sympathetic nervous system may be compensatory, rather than purely pathological, mechanisms in certain contexts. Finally, we show why the described mechanisms are relevant not only in hypertension, but also in the case of healed myocardial infarction.
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